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Task shielding is an important executive control demand in dual-task performance enabling the segregation of stimulus–response translation processes in each task to minimize between-task interference. Although neuroimaging studies have shown activity in left dorsolateral prefrontal cortex (dlPFC) during various multitasking performances, the specific role of dlPFC in task shielding, and whether non-invasive brain stimulation (NIBS) may facilitate task shielding remains unclear. We therefore applied a single-blind, crossover sham-controlled design in which 34 participants performed a dual-task experiment with either anodal transcranial direct current stimulation (atDCS, 1 mA, 20 min) or sham tDCS (1 mA, 30 s) over left dlPFC. Task shielding was assessed by the backward-crosstalk effect, indicating the extent of between-task interference in dual tasks. Between-task interference was largest at high temporal overlap between tasks, i.e., at short stimulus onset asynchrony (SOA). Most importantly, in these conditions of highest multitasking demands, atDCS compared to sham stimulation significantly reduced between-task interference in error rates. These findings extend previous neuroimaging evidence and support modulation of successful task shielding through a conventional tDCS setup with anodal electrode over the left dlPFC. Moreover, our results demonstrate that NIBS can improve shielding of the prioritized task processing, especially in conditions of highest vulnerability to between-task interference.
The ventromedial prefrontal cortex (vmPFC) mediates the inhibition of defensive responses upon encounters of cues, that had lost their attribute as a threat signal via previous extinction learning. Here, we investigated whether such fear extinction recall can be facilitated by anodal transcranial direct current stimulation (tDCS). Extinction recall was tested twenty-four hours after previously acquired fear was extinguished. Either anodal tDCS or sham stimulation targeting the vmPFC was applied during this test. After stimulation ceased, we examined return of fear after subjects had been re-exposed to aversive events. Fear was assessed by reports of threat expectancy and modulations of autonomic (skin conductance, heart rate) and protective reflex (startle potentiation) measures, the latter of which are mediated by subcortical defense circuits. While tDCS did not affect initial extinction recall, it abolished the return of startle potentiation and autonomic components of the fear response. Results suggest hierarchical multi-level vmPFC functions in human fear inhibition and indicate, that its stimulation might immunize against relapses into pathological subcortically mediated defensive activation.